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J Neurophysiol (June 16, 2004). doi:10.1152/jn.00454.2004
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Submitted on May 3, 2004
Accepted on June 8, 2004

Persistent electrical coupling and locomotory dysfunction in the zebrafish mutant shocked

Victor M. Luna1, Meng Wang1, Fumihito Ono1, Michelle R. Gleason2, Julia E. Dallman1, Gail Mandel2, and Paul Brehm1*

1 Neurobiology and Behavior, SUNY at Stony Brook, Stony Brook, New York, USA
2 Neurobiology and Behavior, SUNY at Stony Brook, Stony Brook, New York, USA; Howard Hughes Medical Institute, Stony Brook, New York, USA

* To whom correspondence should be addressed. E-mail: pbrehm{at}notes.cc.sunysb.edu.

Upon initial formation of neuromuscular junctions, slow synaptic signals interact through an electrically coupled network of muscle cells. Following the developmental onset of muscle excitability and the transition to fast synaptic responses, electrical coupling diminishes. No studies have revealed the functional importance of the electrical coupling or its precisely timed loss during development. In the mutant zebrafish shocked (sho) electrical coupling between fast muscle cells persists beyond the time that it would normally disappear in wild type fish. Recordings from sho indicate that muscle depolarization in response to motor neuron stimulation remains slow due to the low pass filter characteristics of the coupled network of muscle cells. Our findings suggest that the resultant prolonged muscle depolarizations contribute to the premature termination of swimming in sho and the delayed acquisition of the normally rapid touch-triggered movements. Thus, the benefits of gap junctions during early synapse development likely become a liability if not inactivated by the time that muscle would normally achieve fast autonomous function.




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